Background Environmental tobacco smoke exposure due to parents is a modifiable risk factor for childhood asthma, but many studies have evaluated parental smoking using self-reported data. Therefore, we aimed to analyze the relationship between parental cotinine-verified smoking status and asthma in their children. Methods This population-based cross-sectional study used data from the Korean National Health and Nutrition Examination Survey from 2014 to 2017. Participants aged 0 to 18 years with complete self-reported physician-diagnosed childhood asthma and measurement of their parental urinary cotinine levels were included. Parental urinary cotinine-verified smoking status was defined using both urinary cotinine levels and self-report, as active, passive, and non-smoker. Sample weights were applied to all statistical analyses because of a complex, multistage and clustered survey design. Logistic regression model was used to analyze the relationship between childhood asthma and parental smoking. Results A total of 5,264 subjects aged < 19 years were included. The prevalence of asthma was 3.4%. The proportions of paternal and maternal urinary cotinine-verified active smokers during the study period were 50.4% and 16.9%, respectively. When parental urinary cotinine level increased, the proportion of parental low household income was increased ( P < 0.001). There was no significant association between the parental urinary cotinine-verified smoking group and childhood asthma group. However, the adjusted odds ratios of childhood asthma in the middle and highest tertile of paternal urinary cotinine levels compared with those in lowest tertile were 1.95 (95% confidence interval [CI], 0.98–3.89) and 2.34 (95% CI, 1.21–4.54), respectively. Conclusion There seems to be a dose-related association between paternal urinary cotinine levels and the risk of childhood asthma. Because of the high rate of paternal smoking, further studies are needed to develop a targeted strategy to reduce parental smoking for childhood asthma.
Polycystic liver disease (PLD) is a hereditary disease characterized by the presence of 20 or more liver cysts. It is classified into three types: isolated autosomal dominant PLD, PLD with autosomal dominant polycystic kidney disease, and PLD with autosomal recessive polycystic kidney disease. Genetic alterations, ciliary dysfunction of the biliary epithelial cells, and aberrant cell signaling pathways are the main factors contributing to the pathophysiology of PLD; however, other complicated mechanisms are also involved. The Gigot and Schnelldorfer classifications are widely used in clinical practice. Most patients with PLD are asymptomatic; however, a few patients with advanced-stage disease may develop symptoms and complications that impair their quality of life and require treatment. The known treatment options for PLD are somatostatin analogues, aspiration with sclerotherapy, fenestration, hepatic resection, and liver transplantation. Although liver transplantation remains the only curative treatment for PLD, medical therapies are gradually being developed with the increasing knowledge of the disease’s pathophysiology. This review focuses on the clinical manifestations and diagnosis of PLD, as well as treatment strategies, to support clinicians regarding the clinical management of the disease.
Drug-induced liver injury is the most common cause of acute liver failure in Western countries by prescription drugs and herbal medications. Liver injury due to azithromycin has rarely been reported. This is a brief report of a patient administered azithromycin and who developed acute liver failure leading to liver transplantation. We report the case of a 68-year-old woman who developed jaundice 1 week after she started taking a azithromycin. On the 3rd day of hospitalization, her hepatic function rapidly deteriorated and level of consciousness decreased to drowsiness. The model for end-stage liver disease score was confirmed to be 33, and liver transplantation was considered. On the 8th day of hospitalization, she underwent emergency living donor liver transplantation, receiving a right lobe liver graft from a 35-year-old male donor, the patient’s son. Currently, she is alive with good liver function after 25 months of transplant. This case suggests that azithromycin may cause rare hepatitis with liver failure. Therefore, at the beginning of the azithromycin treatment, patients should visit the hospital immediately if symptoms such as jaundice and abdominal pain are experienced.
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